Method to reduce SLOSH energy absorption and its damaging effects through the reduction of inelastic collisions in an organism

ABSTRACT

A first embodiment can be a method to reduce SLOSH energy absorption within an organism by reducing the inelastic collisions. A fluid containing organism can utilize an embodiment of the method wherein one or more of reversibly increasing pressure within the organs or cells, reversibly increasing the volume within the organs or cells, reversibly altering vascular, molecular, or cell wall stiffness, or reversibly altering vascular, molecular, or cell wall configuration within said organism may reduce these collisions.

CROSS-REFERENCE TO RELATED APPLICATIONS

This application claims priority from provisional application No.61/241,625 filed on Sep. 11, 2009 and provisional application No.61/260,313 filed on Nov. 11, 2009

STATEMENT REGARDING FEDERALLY SPONSORED RESEARCH OR DEVELOPMENT

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REFERENCE TO SEQUENCE LISTING, A TABLE, OR A COMPUTER PROGRAM LISTINGCOMPACT DISC APPENDIX

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BRIEF DESCRIPTION OF THE SEVERAL VIEWS OF THE DRAWING

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DETAILED DESCRIPTION OF THE INVENTION

When liquid in a tank or vessel experiences dynamic motion, a variety ofwave interactions and liquid phenomena can exist. The oscillation of afluid caused by external force, called sloshing, occurs in movingvessels containing liquid masses, such as trucks, aircraft, and liquidfueled rockets. This sloshing effect can be a severe problem in energyabsorption, and thus, vehicle stability and control. Simply stated, theconcept of this invention is to reduce slosh effects in livingcreatures. The mitigation of blast wave and collision damage is basedlargely on the principle of energy absorption of fluid-filledcontainers. As there becomes more room for movement within a vessel,more energy can be absorbed (SLOSH) rather than transported through thevessel. To reduce this energy absorption, one must attempt to moreclosely approximate elastic collisions. Elastic collisions are thosethat result in no net transfer of energy, chiefly, acoustic, kinetic,vibrational, or thermal (also stated as a coefficient of restitution (r)approximating 1.0). Various embodiments described below may locallyalter, elevate, or temporarily maintain an altered physiology of anorganism to reduce the likelihood of energy absorption through SLOSHwhereby the coefficient of restitution (r) is increased. The coefficientof restitution (r) indicates the variance of an impacting object awayfrom being a complete total elastic collision (an (r) of 1.0=no energytransfer). Blast or energy absorption in an organism can be viewed as acollision of bodies and thus be defined by a transfer of energiesthrough elastic or inelastic collisions. The mechanisms for biologicalfluids and molecules to absorb energy can thus be identified and theresultant means to mitigate that absorption can be achieved throughseveral SLOSH reducing techniques. Dissipation of energies post blast isalso potentiated through these techniques.

An effort to reduce the available space for movement of the brain byincreasing cerebral blood volume can serve the purpose of mitigatingTraumatic Brain Injury (TBI) or increasing orthostatic or G-tolerancethrough SLOSH mitigation at a tissue or organ (macro SLOSH) level. Redblood cells (RBC) or erythrocytes are highly distensible and have a“sloshable” volume to surface area of only 60 percent. Distending orstiffening these erythrocytes can reduce SLOSH within the individualcells at a cellular (micro SLOSH) level and thus reduce energyabsorption upon collision. Molecules themselves have a threedimensionality and can have a lack of cross-bridging providing forfloppy conformational changes that can promote SLOSH. Several mechanismsdisclosed can safely and reversibly alter the conformational state ofcertain structures, cells and molecules in the circulatory system thatwill then reduce energy absorption through SLOSH at a molecular(molecular SLOSH) level. Elevating the local CO₂ and hence lowering thepH environment of an organism can also serve to mitigate SLOSH.

Raised inspired CO₂ (hypercapnia) can mitigate TBI through the reductionof macro SLOSH inside the cranium, but also has the ability to reducethe micro SLOSH inside each individual RBC and reduce the molecularSLOSH of each individual hemoglobin molecule. Each of these physiologychanges allows a better passage of imparted forces through the blood andbrain tissues with less of the forces being absorbed. Within the brain'smore than 150 cc of cerebral blood, there are more than1,000,000,000,000 erythrocytes (1 trillion cells) that hypercapnia canpotentiate to more closely approximate elastic collisions of cells thusreducing the blast or collision energy absorption. Further, ahypercapnic state can also potentiate the collisions of all thehemoglobin molecules present in the cranium and body to be more elastic,thus reducing blast or collision energy absorption. There are 80trillion RBC in the human body, more than one trillion in the brainspace at any one time. All of these cells are susceptible to SLOSHenergy absorption, and that absorption would be reduced in the settingof hypercapnia. Further, there are 240 million molecules of hemoglobininside each RBC. Consequently, there are thus 1.9×10²² hemoglobinmolecules which are able to absorb the energies of a blast. The SLOSHenergy absorption of these molecules can be significantly reduced byhypercapnia altering the molecules to approximate more elasticcollisions.

Hemoglobin is made up of four iron containing heme components and fourglobins that surround (pocket) each heme, and in essence waterproofthese hemes. If the blast energies are absorbed by fluids and bloodcells, they are preferentially absorbed by hemoglobin which is thenconformationally altered to allow water to enter the heme-pocket leadingto a rapid, catalytic oxidation to methemoglobin and superoxide.Superoxide is oxygen with an extra electron; methemoglobin is merely anoxyhemoglobin devoid of a superoxide. Without this extra electron,methemoglobin does not have the ability to carry or transfer oxygen(thus the brain suffocates), and in the case of blast lung, massivelevels of methemoglobin have been recorded. The erythrocytes can slowlyreduce methemoglobin back to functional hemoglobin but if thismethemoglobin reductase reaction is not capable of diverting adequateelectrons to counter this redox chemistry, spillover occurs into theoxidative damaging formation of superoxide, nitric oxide, peroxinitrite,etc. When an electron moves from one molecule to another, the donormolecule is thus oxidized while the receiving molecule is reduced (hencethe term “redox”). For decades methylene blue has been used as theincredibly safe and well tolerated antidote for cyanide poisoning (andmethemoglobinemias). It safely and dramatically facilitates thereductive pathways of methhemoglobin back into hemoglobin. Hypercapnianot only pushes methylene blue into erythrocytes where it can befunctional, but it also appears to actually drive methemoglobinreductase to more quickly convert methemoglobin back to hemoglobin.Further, the anti-oxidants (electron donors) ascorbic acid (vitamin C)and riboflavin are also driven into the erythrocyte by hypercapnia;These antioxidants are not useful for post blast or energy absorptionoutside of erythrocytes. A soldier or athlete can be given physiologicdaily doses of Vitamin C, Riboflavin and methylene blue (not a vitamin)and upon triggering a need, hypercapnia will drive these cofactors intothe erythrocyte where they can mitigate the after effects of blastenergy absorption.

A first embodiment is a method to reduce SLOSH energy absorption throughreduction of inelastic collisions in a fluid containing organism whereinthe method is one or more of reversibly increasing pressure, or volumewithin the organs or cells, or reversibly altering vascular, molecular,or cell wall stiffness or configuration within said organism. Oneembodiment of a method to increase pressure within the cranium can be bytemporarily raising the pCO₂ in the body of the organism by way ofaltering the fractional percentage of CO₂ inspired by the organism. Sucha method can maintain the above hypercapnic inspired CO₂ levels toexceed ambient levels. The CO₂ is actively and instantly pumped intoerythrocytes and after the external CO₂ delivery stops, theintracellular CO₂ levels may take hours to return to normal. Theselevels can be achieved and maintained by an externally impartedrespiratory circuit which can modulate the fractional percentage of CO₂inspired by the organism. The circuit could be one or more of anon-breathing circuit, a breath circuit mask, or a breathing circuitcapable of organizing exhaled gas so as to modulate the fractionalpercentage of CO₂ inspired by the organism (a range from 0.05 to 100%could be utilized). The circuit can include a customizable re-breathingcircuit whose dead space is adjustable based on an individual's weightand estimated tidal volume, and desired or optimized level ofhypercapnia (a pCO₂ range from 25 to 80 mmHg would be optimum). The maskor vessel can incorporate one or several dead space channels or tubesthat provide an inhale and exhale pathway that superimpose each otherand thereby create mixing of inspired and expired gases. Alternatively,a source of fresh gas, potentially containing CO₂ can be supplementedwhen capnography (measurement of exhaled end-tidal CO₂), if utilized, soindicates. A re-breathing respiratory circuit may have one or more ofthe following: a mask or collecting vessel which has one or multiplechannels or tubes whose length or volume is rapidly adjustable toregulate the amount of dead space that an individual will re-breath forthe express purpose of raising or modulating their local CO₂ levelwithin their blood stream. The circuit may also contain aphysiologically insignificant amount of CO₂ in communication with avalve to be delivered to the patient, a fresh gas reservoir incommunication with the source of fresh gas flow for receiving excessfresh gas not breathed by the patient, and a reserve gas supply incommunication with the exit port through the valve and containing CO₂.Alternatively, a non-rebreathing circuit can be comprised of one or moreof the following: a non-rebreathing valve preventing gas exhaled fromthe subject flowing into the circuit, a fresh gas source operative tosupply a fresh gas containing physiologically insignificant amount ofcarbon dioxide to the subject through the non-rebreathing valve, and areserved gas source operative to supply a reserved gas having apredetermined partial pressure of carbon dioxide to the subject throughthe non-rebreathing valve. These respiratory circuits can also be usedto enable organisms to recover more quickly from vapor anestheticadministration, or poisoning with carbon monoxide, methanol, ethanol, orother volatile hydrocarbons. The circuit and method of treatment mayalso be used to reduce nitrogen levels in the body. These additionaluses may require higher concentrations of oxygen than ambient air. Inthis case, the fresh gas could contain 100% oxygen and the reserve gaswould contain 0.04-100% CO₂ and a high concentration of oxygen, forexample 99.96-0%; although simply maintaining a higher pCO₂ is all thatis needed to improve outcomes in carbon monoxide poisoning.

Venous blood returns to the heart from the muscles and organs partiallydepleted of oxygen and containing a full complement of carbon dioxide.Blood from various parts of the body is mixed in the heart (mixed venousblood) and pumped into the lungs via the pulmonary artery. In the lungs,the blood vessels break up into a net of small capillary vesselssurrounding tiny lung sacs (alveoli). The vessels surrounding thealveoli provide a large surface area for the exchange of gases bydiffusion along their concentration gradients. After a breath of air isinhaled into the lungs, it dilutes the CO₂ that remains in the alveoliat the end of exhalation. A concentration gradient is then establishedbetween the partial pressure of CO₂ (pCO₂) in the mixed venous blood(pvCO₂) arriving at the alveoli and the alveolar pCO₂. The CO₂ diffusesinto the alveoli from the mixed venous blood from the beginning ofinspiration (at which time the concentration gradient for CO₂ isestablished) until equilibrium is reached between the pCO₂ in blood fromthe pulmonary artery and the pCO₂ in the alveoli at some time duringbreath. The blood then returns to the heart via the pulmonary veins andis pumped into the arterial system by the left ventricle of the heart.The pCO₂ in the arterial blood, termed arterial pCO₂ (p_(A)CO₂), is thenthe same as was in equilibrium with the alveoli. When the subjectexhales, the end of his exhalation is considered to have come from thealveoli and thus reflects the equilibrium CO₂ concentration between thecapillaries and the alveoli. The pCO₂ in this gas is the end-tidal pCO₂(p_(ET)CO₂). The arterial blood also has a pCO₂ equal to the pCO₂ atequilibrium between the capillaries and alveoli.

With each exhaled breath some CO₂ is eliminated and with eachinhalation, fresh air containing minimal CO₂ (presently 0.04%) isinhaled and dilutes the residual equilibrated alveolar pCO₂ establishinga new gradient for CO₂ to diffuse out of the mixed venous blood into thealveoli. The rate of breathing, or ventilation (V_(E)), usuallyexpressed in L/min, is exactly that required to eliminate the CO₂brought to the lungs and establish an equilibrium p_(ET)CO₂ and p_(A)CO₂of approximately 40 mmHg (in normal humans). When one produces more CO₂(e.g. as a result of fever or exercise), more CO₂ is carried to thelungs and one then has to breathe harder to wash out the extra CO₂ fromthe alveoli, and thus maintain the same equilibrium p_(A)CO₂ but if theCO₂ production stays normal, and one hyperventilates, then excess CO₂ iswashed out of the alveoli and the p_(A)CO₂ falls. There are manyscenarios in which we wish the inspired CO₂ to be greater than thatwhich would normally come about physiologically. This heightened stateof CO₂ in the system has many protective benefits but certainly onewould not want to allow the increase in CO₂ to rise to dangerous levels.

One way to contribute to the pCO₂ levels of the organism can be by thedelivery of one or more medicaments that are known to alter pH of theorganism such as carbonic anhydrase inhibitors. Some examples ofcarbonic anhydrase inhibitors are Topiramate, Methazolamide, Dorzolamideor Acetazolamide. Carbonic anhydrase inhibitors can act as milddiuretics by reducing NaCl and bicarbonate reabsorption in the proximaltubule of the kidney. The bicarbonaturia will thus produce a metabolicacidosis. This mild acidosis has many potential benefits in mitigatingSLOSH as described within. Anticipated acidic pH changes that wouldprove beneficial would be between about 7.30 and 7.40. Associated pCO₂levels would quate to pCO₂ levels of about 45 to 60 mmHg.

Another embodiment of elevating pCO₂ in the body of an organism can be abreathing circuit that maintains an elevated pCO₂. A circuit canmaintain an estimated yet elevated end tidal pCO₂ by interposing one ormore channels or tubes through which the individual breathes that causesa re-breathing of their previous inhaled or exhaled breath. Thesechannels allow a mixing of inhaled ambient gas and exhaled alveolar gas.The optimal amount of gas re-breathed can be determined by estimatingthe individual's weight in kilograms and multiplying it by a factor,such as 7, to arrive at an estimated tidal volume in cm³. In oneembodiment a third of this volume can be added to the breathing circuitas dead space. This volume determines the predicted level of end tidalCO₂ to which the device will equilibrate. Alternatively a secondarysource of CO₂ could be interposed to rapidly, and on demand, increasethe percentage of inspired CO₂. Several paper or thin walled tubes orchannels can extend away from the enclosed mouth and nose portion of thedevice and/or several regions can be placed sequentially along thechannels or tubing as perforations or weakening points so as theindividual will be able to tear, cut, or break off a predeterminedamount of the tubing and thus precisely alter the remaining dead spaceof the circuit. Demarcations and identifiers placed along thechannels/tubing can help the individual decide at which perforation orweakened zone to tear, cut, or remove. Again, these can be determined asfollows: Tidal volume can be estimated by measuring one's weight inkilograms and multiplying by 7, the result would be in cm³ of tidalvolume. To determine the amount of dead space to add to the outflowtract of the mask, one need only take the resultant tidal volume and adda corresponding percentage of the tidal volume (say 33%) to the outflowtract of the mask. Each incremental increase in dead space added to theoutflow tract would cause an incremental increase in final pCO₂. Forexample, if the weight of the individual is 120 kg then the estimatedtidal volume would be 840 cm³. We would want the individual to re-breatha portion of that tidal volume equating to 33% of this which equals 277cm³. This added volume of dead space would be expected to increase thepCO₂ by approximately 7-8 mmHg.

In addition to the adjustable dead space, monitoring the end tidal CO₂and driving the export valve to open or close to alter the source of thenext inspired breath may be utilized in settings whereby preciseknowledge of end tidal CO₂ may be required. For example if an end tidalCO₂ desired range is 45 mmHg, then upon noting the end tidal CO₂ beingonly 35 mmHg, the valve would be directed to close requiring theindividual to take the next breath from the adjustable dead spacereservoir/tubing that a previous breath had been collected into. Thisexpiration typically has 4-5% CO₂ within it allowing a greater inspiredCO₂ on the next breath. A reservoir can act as a buffer to store extraCO₂ gas. Even when ventilation increases, the subject breaths theaccumulated elevate CO₂ gas allowing pCO₂ to rise to the desired level.A circuit to maintain normal CO₂ can include a non-rebreathing valve, asource of fresh gas, a fresh gas reservoir and a source of gas to beinhaled, such as from the increased dead space region or a reservoir ofhigher concentration of CO₂.

The method of controlling pCO₂ in a patient at a predetermined desiredlevel can be provided comprising a breathing circuit/mask which iscapable of increasing the CO₂ to enable an increase in cerebral bloodflow and resultant cerebral blood pressure. With increased cerebralblood flow, cerebral blood velocity, and intracranial pressure thereremains less space for intracranial tissues to move in relation to eachother, thus brain pulsitility and SLOSH is diminished. This wouldrequire minimizing compressibility at air/fluid/tissue junctures.Although brain tissue is thought to be incompressible and fluid/blood isalso relatively incompressible, the fluids are able to escape throughthe vessels and allow to and fro movement within the cranium and thusabsorption of blast wave energies. If either the elevated CO₂ has beentriggered with a resultant increase in cerebral blood flow and/or therehas been increased intracranial pressure by any means before a traumaticevent, the brain and its components would be less prone to slosh aroundwithin the cranium and in relation to each individual component (thusbetter approximating elastic collisions). This is not unlikeseat-belting a passenger inside an automobile. Further, if TBI were tooccur despite the above restraining effects of the increased cerebralblood flow, an elevated CO₂ would even serve to optimize the healingenvironment of the brain tissue itself by reducing the systemicinflammatory response and maximizing flow of oxygen rich hemoglobinwhich is more capable of delivering its oxygen due to high levels of CO₂through maximizing the oxy-hemoglobin dissociation curve.

SLOSH absorption may also be reduced by reversibly increasing pressureor volume within the organs or cells of the organism. The intracranialvolume and pressure can be reversibly increased by a device that reducesthe flow of one or more outflow vessels of the cranium of said organism.This device would necessarily need to compress the vessels at a levelsurpassing venous pressure (approximately 15 mmHg, yet not surpassarterial pressure of approximately 80 mmHg). Intracranial volume canalso be reversibly increased by the delivery of one or more medicamentsto facilitate an increase in intracranial volume or pressure includingbut not limited to Minocycline, insulin-like growth factor 1, Provera,and Vitamin A.

The human erythrocyte is very distensible and, as such, is particularlycapable of absorbing energies imparted into it by suffering inelasticcollisions. Mathematical analysis of Newton's Cradle shows thatinelastic collisions absorb energy as heat and kinetic energy whereaselastic collisions serve to allow the forces to pass through withoutimparting as much energy. However, triggering an increase in pCO₂ in theblood and serum (resulting in erythrocytes pumping the CO₂ into thecytoplasm), can serve to cause nearly an immediate increase inbicarbonate created within the erythrocyte creating an osmotic swellingof fluid into the cell and reducing SLOSH absorption. Further, the wallsof erythrocytes that have been exposed to higher levels of CO₂ have beenshown to be less distensible; and also if swollen, they shouldfacilitate more elastic collisions when forces are imparted into them.Even after the mechanism that supplies extra CO₂ has been removed, itwill take hours for the cells to equilibrate back to pre-hypercapnialevels. This would further serve to reduce force impartation into thebrain or any erythrocyte perfused structures. The reversible swelling ofthe cells and the altered red cell membrane's distensibility would alsoserve to mildly reduce the shear thinning capability that bloodtypically exhibits and again, this would serve to better approximateelastic collisions when forces are imparted.

In addition to increasing the volume within the cell one can alsoreversibly alter the vascular, molecular, or cell wall configurationwithin the organism to reduce SLOSH energy absorption. The configurationof the cell wall can be reversibly altered to increase membranestability and decrease membrane fluidity. The addition of one or more ofDHA and Magnesium oxide can be used to alter erythrocyte cell wallconfiguration. Typical DHA supplementations would be in the order of50-1000 mg orally a day and MgO of 50-1000 mg orally a day. Theconfiguration of hemoglobin can also be reversibly altered by alteringone or more of pH (to a pH of about 7.0 to 7.5), pCO₂ (to pCO₂ of about25 to 80 mmHg) or blood levels of 2,3-Bisphosphoglycerate (to about 6.0to 1000 μmol/mL) within the organism to decrease hemoglobin elasticityand fluidity. 2,3-Bisphosphoglycerate levels may be increased by methodssuch as phosphate loading.

Another embodiment can be a compression device to reduce the likelihoodof energy absorption to the brain through raising intracranial and intraocular volume and pressure by applying pressure to the outflowvasculature and/or cerebral spinal fluid of the brain. The result wouldbe an increase in the structure's coefficient of restitution (r) byattaching a cinch or collar around the neck of the individual ororganism. The compression device can be of any design including, but notlimited to, a band or cord.

Safely and reversibly increasing cerebral blood volume by any amount upto 10 cm³ and pressure by any amount up to 70 mmHg would serve to fillup the compliance of the cerebral vascular tree and thus reduce theability to absorb external energies through SLOSH energy absorption.“With the application of measured pressure to the neck, the cranialblood volume increases rapidly and plateaus at a new higher level. Moyeret al reported that cerebral arterial blood flow was not affected byobstructing the venous outflow of blood from the brain.”¹ “The bloodvolume venous pressure relationship shows a diminishing increase involume with each increment of neck pressure over the range 40 to 70 mmof mercury. It is of interest that the cranial blood volume increasesfrom 10 to 30 per cent (with this neck pressure).”² The cerebral spinalfluid pressure responds on compression of the individual jugular veins.“The average rise was 48 per cent.”³ Jugular compression increasescerebral blood flow to a new plateau in as little as 0.5 seconds.^(4, 5)This degree of cranial blood volume and pressure increase would be verybeneficial in SLOSH mitigation. Although lesser cranial pressure andvolume increases may still have beneficial effects, an increase of 3 cm³volume and 5 mm Hg is a baseline goal.

Further, safety of such a procedure of venous compression is quiteabundant in the literature as it mirrors the 100 year old QuenkenstadtManeuver. In this maneuver, “the compression of the neck does notinterfere with arterial flow into the cranium. Although the venousjugular flow beneath the pressure cuff may be temporarily halted, thevenous outflow from the cranium is never completely stopped,particularly from the anastomosis between the spinal vein and thebasilar plexus and occipital sinuses which are incompressible.”^(6, 7)In fact, there was no correlation between Electroencephalographic (EEG)changes or changes in systolic arterial blood pressure occurring duringjugular compression.⁸ Thus, neck compression of up to 70 mmHg does notaffect cardiac output, arteriolar blood pressure, pulse rate, or urineflow.

The compression device may be of any material including but not limitedto elastic materials. Elastic materials can be any material which whenstretched will attempt to return to the natural state and can includeone or more of textiles, films (wovens, non-wovens and nettings), foamsand rubber (synthetics and natural), polychloroprene (e.g. Neoprene),elastane and other polyurethane-polyurea copolymerss (e.g. Spandex,Lycra), fleece, warp knits or narrow elastic fabrics, raschel, tricot,milanese knits, satin, twill, nylon, cotton tweed, yarns, rayon,polyester, leather, canvas, polyurethane, rubberized materials,elastomers, and vinyl. There are also a number of elastic materialswhich are breathable or moisture wicking which may be preferable duringextended wearing periods or wearing during periods of exercise. Inaddition the compression device could be partially constructed, coated,or constructed of one or more protecting materials such as Kevlar(para-aramid synthetic fibers), Dyneema (ultra-high-molecular-weightpolyethylene), ceramics, or shear thickening fluids.

The device may encompass circumferentially, the entire neck or justpartially around the neck, yet still providing partial or totalocclusion of one or more of the outflow vessels on the neck,specifically, but not limited to the internal and external jugularveins, the vertebral veins, and the cerebral spinal circulation. Thedevice may encompass horizontally, the entire neck or just partially upand down the neck.

The width of the compression device may range from a mere thread (at afraction of an inch) to whatever the length of the exposed neck (up to12 inches in humans or greater in other creatures), the length may rangefrom 6 to 36 inches to circumnavigate the neck. The width of thecompression device could be as small as ¼ inch but limited only by theheight of the neck in largest width, which would be typically less than6 inches. The thickness of said device could range from a film beingonly a fraction of a millimeter to a maximum of that which might becumbersome yet keeps ones neck warm such as 2-3 inches.

The compression device may be preformed for the user in a circularconstruct. This one size fits all style can have a cinch of sorts thatallows one to conform the device to any neck region. Alternatively thecompression device may be a first and second end which is connected by afastener. A fastener may be a hook and ladder attachment, a snap, abutton or any of a number of attachment mechanisms that would be knownto one skilled in the art. A compression device with a fastener couldhave a release mechanism whereby the device can break open or apart at apredetermined force to prevent the collar from inadvertently beingsnagged or compressing too tightly. One quick release or automaticrelease method would be the applying of small amounts of hook and ladderattachments within the circumferential ring which would shear apart upontoo much force being applied to the compression device.

The compression device may also have one or more monitoring devicesand/or communication devices attached or embedded. The compressiondevice can also have a pocket or pouch attached depending on the heightof the compression device used. Certainly, advertising can be imprintedor emblazoned onto the device.

These terms and specifications, including the examples, serve todescribe the invention by example and not to limit the invention. It isexpected that others will perceive differences, which, while differingfrom the forgoing, do not depart from the scope of the invention hereindescribed and claimed. In particular, any of the function elementsdescribed herein may be replaced by any other known element having anequivalent function.

¹ MOYER, J. H., MILLER, S. I. AND SNYDER, H.: Effect of IncreasedJugular Pressure on Cerebral Hemodynamics. I. Appi. Physiol. 7:245,1954.

² The Elasticity of the Cranial Blood Pool, Masami Kitano, M.D., WilliamH. Oldendorf, M.D.: C and Benedict Cassen, Ph.D., JOURNAL OF NUCLEARMEDICINE 5:613-625, 1964

³ Observations on the C.S.F Pressure during Compression of the JugularVeins, D. A. J. Tyrrell, Postgrad. Med. J. 1951;27;394-395

⁴ The Elasticity of the Cranial Blood Pool Masami Kitano, M.D., WilliamH. Oldendorf, M.D.: C and Benedict Cassen, Ph.D., JOURNAL OF NUCLEARMEDICINE 5:616, 1964

⁵ A Cinemyelographic Study of Cerebrofluid Dynamics Amer J of Roent,GILLAND et al. 106 (2): 369. (1969)

⁶ BATSON, 0. V.: Anatomical Problems Concerned in the Study of CerebralBlood Flow. Fed. Proc. 3:139, 1944

⁷ GREGG, D. E. ANDSHIPLEY, R. E.: Experimental Approaches to the Studyof the Cerebral Circulation. Fed. Proc. 3:144, 1944.

⁸ Changes in the electroencephalogram and in systemic blood pressureassociated with carotid compression, Fernando Tones, M.D. and AnnaEllington, M.D. NEUROLOGY 1970;20:1077

What is claimed is:
 1. A method to reduce SLOSH energy absorption in thebrain of a subject sustaining a traumatic event selected from the groupconsisting of a blast wave and collision event, comprising applying15-80 mmHg of pressure to one or more neck veins of the subject beforeand during the traumatic event, wherein the pressure on the one or moreneck veins is sufficient to reduce SLOSH energy absorption by the brainduring the traumatic event by increasing the intracranial pressure,intracranial blood volume, or both.
 2. The method of claim 1, whereinthe pressure on the one or more neck veins is not more than 40 mm Hg. 3.The method of claim 1, wherein one of the neck veins is the internaljugular vein.
 4. The method of claim 1, wherein one of the neck veins isthe external jugular vein.
 5. The method of claim 1, wherein pressure isapplied using a compression device.
 6. The method of claim 5, whereinthe compression device does not apply a compression pressure of greaterthan 70 mm Hg to the one or more neck veins.
 7. A method for mitigatingtraumatic brain injury in a subject sustaining a traumatic eventselected from the group consisting of a blast wave and collision event,comprising applying 15-80 mmHg to one or more neck veins of the subjectbefore and during the traumatic event, wherein the pressure on the oneor more neck veins is sufficient to mitigate a traumatic brain injurycaused by the traumatic event by increasing the intracranial pressure,intracranial blood volume, or both.
 8. The method of claim 7, whereinthe pressure on the one or more neck veins is not more than 40 mm Hg. 9.The method of claim 7, wherein one of the neck veins is the internaljugular vein.
 10. The method of claim 7, wherein one of the neck veinsis the external jugular vein.
 11. The method of claim 7, whereinpressure is applied using a compression device.
 12. The method of claim11, wherein the compression device does not apply a compression pressureof greater than 70 mm Hg to the one or more neck veins.